摘要: Host anti-viral innate immunity plays important roles in the defense against HSV-1 infection. In this study, we find an unexpected role for innate LT/LIGHT signaling in promoting HSV-1 replication and virus induced inflammation in immunocompromised mice. Using a model of footpad HSV-1 infection in Rag1-/-mice, we observed that blocking LT/LIGHT signaling with LT beta R-Ig could significantly delay disease progression and extend the survival of infected mice. LT beta R-Ig treatment reduced late proinflammatory cytokine release in the serum and nervous tissue, and inhibited chemokine expression and inflammatory cells infiltration in the dorsal root ganglia (DRG). Intriguingly, LT beta R-Ig treatment restricted HSV-1 replication in the DRG but not the footpad. These findings demonstrate a critical role for LT/LIGHT signaling in modulating innate inflammation and promoting HSV-1 replication in the nervous system, and suggest a new target for treatment of virus-induced adverse immune response and control of severe HSV-1 infection.
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期刊:
SCIENTIFIC REPORTS
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分类:
生物学
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生物物理学
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引用:
ChinaXiv:201605.01307
(或此版本
ChinaXiv:201605.01307V1)
DOI:10.12074/201605.01307V1
CSTR:32003.36.ChinaXiv.201605.01307.V1
- 推荐引用方式:
Liang, Yong,Yang, Kaiting,Guo, Jingya,Peng, Hua,Liang, Yong,Yang, Kaiting,Wroblewska, Joanna,Fu, Yang-Xin,Wroblewska, Joanna,Fu, Yang-Xin.(2016).Innate lymphotoxin receptor mediated signaling promotes HSV-1 associated neuroinflammation and viral replication.SCIENTIFIC REPORTS.[ChinaXiv:201605.01307]
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